Basal Ganglia Calcification and Pulmonary Embolism in Catatonia

“Mr. B” was a 31-year-old white man with schizophrenia who presented to the emergency room with refusal of oral intake, and severe psychomotor retardation and posturing. Two days prior, the patient developed paranoid, auditory hallucinations, and became depressed. At baseline he was not taking any medication and was able to function with assistance from his brother. Patient was obese (BMI=50.2), but otherwise his medical and family history was unremarkable.

His present evaluation was remarkable for confusion, depressed mood, rigid posture, and hypoactive motor level. Patient was “not answering any questions.” He exhibited catatonic features, such as mutism, posturing, anorexia, and extreme negativism. His vital signs were within normal limits. Physical exam revealed a stuporous individual, unresponsive to commands or noxious stimuli, with brisk reflexes, and fixed and unblinking stare. EEG demonstrated a small amount of right temporal activity without any features suggestive of encephalitis or epilepsy. ECG shows sinus rhythm, no ischemic changes, with a QTc interval of 0.47 sec.

On day 3, patient was transferred to the ICU for loss of consciousness and hypoxia. A computed tomogram (CT) of the head revealed bilateral basal ganglia calcifications, greater on the left than right. D-dimer was 5964 (normal range<500 ng/ml), and CT chest angiogram was conclusive for PE. Transthoracic Echocardiogram captured a clot in transit through the patent foramen ovale. Laboratory testing was otherwise unremarkable, including serum calcium (9.8 mg/dl), parathyroid hormone (17 pg/ml), hemoglobin A1C (5.5%), and a negative hypercoagulable workup.

Therapeutic anticoagulation was achieved with heparin then warfarin. Patient was also administered low dose lorazepam to suspend catatonic features.

This case adds to other reports 1, 3 of psychotic features and catatonia associated with calcification of basal ganglia pathways. Catatonia in schizophrenia maybe determined by a disruption in the thalamo-cortico-striatal circuits. In this case, the calcification is neither associated with calcium nor parathyroid disorders. 3

The risk of fatal pulmonary embolism is inherent in catatonic symptoms. A previous study 4 suggests death from PE would occur after the second week of catatonic symptoms and often occurred without warning. Our case adds that in an obese schizophrenia male with no hypercoagulability and past medical history, pulmonary embolism may actually occur within the first week of catatonia.

Patients with catatonia are likely to develop PE as a result of deep venous thrombosis from immobility. While a study 5 has suggested complete anticoagulation during immobility would be beneficial, the role of anticoagulant medications in catatonic patients is unclear. 4 Our case adds that treating catatonia with benzodiazepines, along with DVT/PE prophylaxis, would likely prevent catastrophic outcome.